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Age-related macular degeneration (AMD) is the most common cause of irreversible central vision loss in elderly patients. Dilated funduscopic findings are diagnostic; color photographs, fluorescein angiography, and optical coherence tomography assist in confirming the diagnosis and in directing treatment. Treatment is with dietary supplements, intravitreal injection of antivascular endothelial growth factor drugs, laser photocoagulation, photodynamic therapy, and low-vision devices.
AMD is the leading cause of permanent, irreversible vision loss in the elderly. It is more common among whites.
Etiology
Risk factors include the following:
Pathophysiology
Two different forms occur:
Although only 10% of patients with AMD have the wet form, 80 to 90% of the severe vision loss caused by AMD results from wet AMD.
Dry AMD causes changes of the retinal pigment epithelium, typically visible as dark pinpoint areas. The retinal pigment epithelium plays a critical role in keeping the cones and rods healthy and functioning well. Accumulation of waste products from the rods and cones can result in drusen, which appear as yellow spots. Areas of chorioretinal atrophy (referred to as geographic atrophy) occur in more advanced cases of dry AMD. There is no elevated macular scar (disciform scar), edema, hemorrhage, or exudation.
Wet AMD occurs when new abnormal blood vessels develop under the retina in a process called choroidal neovascularization (abnormal new vessel formation). Localized macular edema or hemorrhage may elevate an area of the macula or cause a localized retinal pigment epithelial detachment. Eventually, neovascularization causes a disciform scar under the macula.
Symptoms and Signs
Dry AMD:
The loss of central vision occurs over years and is painless, and most patients retain enough vision to read and drive. Central blind spots (scotomas) usually occur late in the disease and can sometimes become severe. Symptoms are usually bilateral.
Funduscopic changes include the following:
Wet AMD:
Rapid vision loss, usually over days to weeks, is more typical of wet AMD. The first symptom is usually visual distortion, such as a central blind spot (scotoma) or curving of straight lines (metamorphopsia). Peripheral vision and color vision are generally unaffected; however, the patient may become legally blind (< 20/200 vision) in the affected eye or eyes, particularly if AMD is not treated. Wet AMD usually affects one eye at a time; thus, symptoms of wet AMD are often unilateral.
Funduscopic changes include the following:
Diagnosis
Both forms of AMD are diagnosed by funduscopic examination. Visual changes can often be detected with an Amsler grid (see Approach to the Ophthalmologic Patient: Visual field testing). Color photography and fluorescein angiography are done when findings suggest wet AMD. Angiography shows and characterizes subretinal choroidal neovascular membranes and can delineate areas of geographic atrophy. Optical coherence tomography (OCT) aids in identifying intraretinal and subretinal fluid and can help assess response to treatment.
Treatment
Dry AMD:
There is no way to reverse damage caused by dry AMD. Patients with extensive drusen, pigment changes, and/or geographic atrophy can reduce the risk of developing advanced AMD by 25% by taking daily supplements of the following:
Vitamin A is sometimes substituted for β-carotene. In smokers, β-carotene and vitamin A can increase the risk of lung cancer. For this reason, these supplements are contraindicated in patients who have smoked in the previous 7 yr. All patients who take these supplements have an increased risk of hospitalization for GU tract symptoms. Some patients also have yellowing of the skin. Reducing cardiovascular risk factors as well as regularly eating foods high in ω-3 fatty acids and dark green leafy vegetables may help slow disease progression.
Wet AMD:
Patients with unilateral wet AMD should take the daily nutritional supplements that are recommended for dry AMD to reduce the risk of AMD-induced vision loss in the other eye. The choice of other treatments depends on the size, location, and type of neovascularization. Intravitreal injection of antivascular endothelial growth factor (anti-VEGF) drugs (usually ranibizumab, bevacizumab, aflibercept, or, occasionally, pegaptanib sodium) can substantially reduce the risk of vision loss and can help restore reading vision in up to one third of patients. In a small subset of patients, thermal laser photocoagulation of neovascularization outside the fovea may prevent severe vision loss. Photodynamic therapy, a type of laser treatment, also helps under specific circumstances. Corticosteroids (eg, triamcinolone) are sometimes injected intraocularly along with an anti-VEGF drug. Other treatments, including transpupillary thermotherapy, subretinal surgery, and macular translocation surgery, are seldom used.
Supportive measures:
For patients who have lost central vision, low-vision devices such as magnifiers, high-power reading glasses, large computer monitors, and telescopic lenses are available. Also, certain types of software can display computer data in large print or read information aloud in a synthetic voice. Low-vision counseling is advised.
Key Points
Last full review/revision December 2012 by Sunir J. Garg, MD, FACS
Content last modified January 2013
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